Korean J Obes.
2011 Jun;20(2):45-50.
Obesity and ER Stress
- Affiliations
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- 1Department of Molecular Cell Biology and Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Korea. shkoo@skku.edu
Abstract
- Endoplastic reticulum (ER) is one of the cellular organelle found in all eukaryotes. It plays a critical role in the protein folding, lipid and sterol biosynthesis, and the storage of intracellular calcium. Unfolded protein response (UPR) refers to the collective signaling cascades that is activated in response to the malfunction of ER, and is responsible for either promoting apoptosis or promoting survival of the affected cells or organisms. Normally, UPR protects the function of ER by enhancing the induction of proper folding of proteins, degrading misfolded proteins, and reducing the general protein synthesis by decreasing the activity of general translational machinery. However, UPR has been shown to be a major culprit in invoking insulin resistance and other more severe metabolic diseases under the state of chronic ER stress in response to obesity caused by high fat diet. In this review, we would like to discuss the molecular mechanism for the promotion of metabolic diseases by obesity-mediated physiological chronic ER stress.